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GI > Hepatobiliary UWorld: Path, Physio, Pharm > Flashcards

Hepatobiliary UWorld: Path, Physio, Pharm Flashcards

0
Q

What is the marker for HCC?

A

alpha-fetoprotein (AFP)

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1
Q

3 major etiologies of hepatocellular carcinoma

A

Viral infection with hep B or C
Chronic alcoholism
Food contaminants (aflotoxin)

Cirrhosis is not required for dx but seems to be a major contributor

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2
Q

Hemtemesis, palpable spleen, esophageal varices, portal hypertension, no abnormalities on liver biopsy. Dx?

A

Portal vein thrombosis. (Long-term alcohol would show cirrhosis on biopsy)

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3
Q

Crigler-naijar syndrome

A

Autosomal recessive absence of liver conjugation enzymes. Causes unconjugated hyperbilirubinemia. UCB cannot be excreted, so builds up in tissues like the brain, causes bilirubin encephalopathy.

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4
Q

Kernicterus

A

Bilirubin encephalopathy, potentially fatal condition with severe jaundice and neurological impairment. UCB builds up in basal ganglia

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5
Q

Dubin-Johnson syndrome

A

Autosomal recessive absence of biliary transport protein, defective liver excretion. Causes conjugated bilirubinemia, benign except for black liver.

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6
Q

Rotor syndrome

A

Like Dubin-Johnson but milder: defect of biliary transport protein, defective liver excretion. Causes conjugated bilirubinemia, benign and NO black liver

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7
Q

Lab tests that assess liver function

A

prothrombin time, bilirubin, albumin, cholesterol

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8
Q

Lab tests that assess structural/cellular integrity of liver

A

Transaminases (AST, ALT)

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9
Q

Lab tests that assess biliary tract

A

Alkaline phosphatase (nonspecific, found in lots of tissues), gamma glutamyl transferase (more specific)

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10
Q

Elevated alkaline phosphatase: what is next thing to check?

A

gamma glutamyl transpeptidase

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11
Q

What is acute cholecystitis? Main cause?

A

Acute inflammation of gallbladder, initiated by obstruction of gallbladder neck or cystic duct. This is the major complication of cholelithiasis

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12
Q

Gilbert syndrome

A

Mild familial decrease in UDG conjugation enzyme. Only clinical sign is jaundice in times of stress: fasting, fever, hemolysis, fatigue, exertion.

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13
Q

Treatment of acetominophen overdose, mechanism

A

N-acetyl cysteine, binds toxic metabolite and provides sulfhydryl groups to sulfonate and metabolize

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14
Q

Antidote in iron poisoning

A

Deferoxamine

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15
Q

“Serum sickness”, malaise, fever, skin rash, pruritis, lymphadenopathy, joint pain. Followed by anorexia, jaundice, RUQ pain.

A

Acute viral Hep B

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16
Q

Acute viral hepatitis labs

A

Significant elevations in ALT and AST (ALT>AST), rise in bilirubin and alk phos

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17
Q

What tests do you need to do for pt on statins

A

LFTs

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18
Q

Most common malignant hepatic lesion

A

Metastasis

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19
Q

Black pigment stones

A

Gallstones seen in chronic extravascular hemolysis. Usually small, spiculated, crumbly, and radioopque. Form when UCB precipitates as calcium bilirubinate.

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20
Q

Significant risk factor for cholesterol stones, black pigment stones, brown pigment stones

A

Cholesterol: Obesity, Crohn, CF, age, estrogen, drugs
Black: hemolysis
Brown: infection

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21
Q

Mechanism of damage in hepatic steatosis

A

Increased activity of dehydrogenase enzymes –> increased NADH –> decreased fatty acid oxidation.

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22
Q

Possible outcomes of hep B infection

A
  • Acute hepatitis with complete resolution (95%)
  • Chronic hepatitis (with or without cirrhosis)
  • Fulminant hepatitis with massive liver necrosis
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23
Q

HIDA scan

A

Nadionuclide scan, used for dx of acute cholecystitis. If you don’t see gall bladder on the scan, the cystic duct is obstructed and it is a positive test result.

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24
Q

Gross and histo findings in Dubin-Johnson syndrome

A

Gross: black liver
Histo: normal, may see dense pigment with epinephrine metabolites within lysosomes

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25
Q

Middle aged woman, insidious onset, pruritis, fatigue, hepatosplenomegaly, jaundice, steatorrhea, portal htn osteopenia. Elevated alk phos and cholesterol. Serum anti mitochondrial antibodies. Maybe associated with autoimmune disease

A

Primary biliary cirrhosis

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26
Q

Primary biliary cirrhosis pathophys

A

Autoimmune destruction of intrahepatic bile ducts and cholestatis.

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27
Q

Primary biliary cirrhosis: associations

A

Sjogren syndrome, CREST, Raynaud’s, RA, celiac, thyroid disease

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28
Q

Hepatitis B: risk of hepatocellular carcinoma?

A

Increased. Virus integrates DNA into host genome

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29
Q

Main mechanism of excess copper removal (healthy)

A

In liver, incorporated into ceruloplasmin. Some goes into plasma (most of circulating copper), some is excreted via bile, stool.

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30
Q

Mechanism of damage in viral heptitis

A

Infected hepatocytes display viral antigens on MHC 1, and CD8 T-cells destroy.

31
Q

Neuro symptoms, elevated transaminases, decreased serum ceruloplasmin

A

Wilson’s disease. Tx is penicillamine

32
Q

Acute acalculous cholecystitis

A

Acute inflammation of gallbladder in absence of gall stones. Secondary to stasis and ischemia.

Seen in hospitalized pts with: sepsis, immunosuppression, trauma, burns, DM, infxn, surgery.

33
Q

Middle aged female with long history of pruritis and fatigue who develops pale stool and xanthelasma. Classic picture of

A

primary biliary cirrhosis

34
Q

Pt with HBV develops hepatocellular carcinoma. What is the trigger?

A

Integration of viral DNA into host genome: activates insulin-like growth factors and proliferation, and suppresses p53.

35
Q

Pathogenesis of biliary atresia

A

Complete obstruction of extrahepatic bile ducts, due to failure to form or destruction of biliary tree

36
Q

Presentation, labs, liver biopsy of biliary atresia

A

P: Jaundice, dark urine, firm enlarged liver in first 3 months of life

L: Increased direct bilirubin (CB), alk phos, gamma glutamyltransferase

B: Intrahepatic duct proliferation, portal tract edema and fibrosis, paranchymal fibrosis

37
Q

Where does copper deposit in Wilson’s?

A

Cornea (Kayser-Fleischer rings), basal ganglia (neuro symptoms)

38
Q

Hepatic encephalopathy

A

Reversible decline in neurologic function precipitated by hepatic damage. Often set off by stressor. Failure of liver to metabolize waste products –> increased ammonia in circulation.

39
Q

Hemochromatosis is a disease of

A

intestinal absorption of iron. Loss of regulation of enterocytes –> too much absorption.

40
Q

A1AT deficiency on liver biopsy

A

Red/pink PAS+ granules of unsecreted, polymerized A1AT in periportal hepatocytes

41
Q

Increased estrogen in cirrhosis comes from? Causes?

A

Hyperestrinism is from liver’s inability to metabolize estrogens and increased sex hormone-binding globulin –> estrogen excess state.

Testicular atrophy, gynecomastia, spider angiomata

42
Q

End stage liver disease - gross liver

A

Cirrhosis. Diffuse firosis, nodular parenchymal regeneration replaces lobular architecture.

43
Q

Hemochromatosis causes iron overload in:

A

heart, pancreas, liver

44
Q

Hep B: biopsy

A

Cytoplasm filled with spheres and tubules of HBsAg, fine granular eosinophilic “ground glass” appearance.

45
Q

HBV vs HCV

A

B: Ballooning degeneration, hepatocyte necrosis, portal inflammation, ground glass cytoplasm appearance

C: Lymphoid aggregates within portal tracts, focal areas of macrovesicular steatosis

46
Q

A 45 y/o Caucasian male has slow/incomplete gallbladder emptying in response to CCK. He is likely to develop:

A

biliary sludge

47
Q

Aflatoxins cause

A

hepatocellular carcinoma via a p53 mutation

48
Q

Administration methods to avoid first pass metabolism

A

IV, sublingual, rectal

49
Q

Elderly female with waves of abdominal pain, nausea, vomiting. Air in biliary tree, hard mass with high cholesterol content in ileocecal valve

A

Gallstone ileus. Large gallstone erodes into intestinal lumen, fistula between gallbladder and intestine. Intermittent obstruction (waves of symptoms), eventually stuck in ileum.

50
Q

What are the worst prognostic indicators in cirrhosis?

A

Prolonged PT, hypoalbuminemia, these are indicators of liver function

Note: AST, ALT are indicators of hepatocellular damage but not failure.

51
Q

Isoniazid toxicity

A

Anti-TB, decreases synthesis of mycolic acids. Neurotoxicity, hepatotoxicity, transient increases in AST and ALT

INH Injures Neurons and Hepatocytes

52
Q

21 y/o, Impaired balance, difficulty speaking, onset over a few months, elevated transaminases, no dugs or alcohol.

A

Wilson’s disease. Do slit lamp check

53
Q

Fluid filled cavity in liver, fever chills and RUQ pain

A

Hepatic abscess. Can occur via s aureus seeding hematogenously, or enteric bacteria ascending biliary tract.

54
Q

Pathogenesis of cholesterol gallstones

A

Increased cholesterol, decreased bile acids and phospholipids –> bile becomes supersaturated –> nucleation, aggregation promoted by mucus hypersecretion, calcium salts, hypomotility –> stone

55
Q

3 drugs that increase risk for cholesterol gallstones

A

Fibrates (esp with bile acid resins), octreotide, ceftriaxone

56
Q

How do fibrate cause cholesterol stones?

A

Suppression of 7a-hydroxylase activity reduces conversion to bile acids, excess secretion of cholesterol into bile

57
Q

Cholestasis relation to osteomalacia?

A

Causes ADEK deficiency, so D deficiency is associated with osteomalacia (reduced bone density because of decreased mineralization)

58
Q

Causes of cholestasis

A
  • 2ndary to hepatocellular dysfunction
  • Intrahepatic obstruction: drug induced, primary biliary cirrhosis, pregnancy, primary sclerosing cholangitis
  • Extrahepatic obstruction: Choledocholithiasis, malignancy
59
Q

First order vs zero order kinetics

A

First order: dose dependent, constant proportion metabolized
Zero order: dose independent, constant amount metabolized

When a drug reaches saturation, it switches to zero order

60
Q

Most common benign liver tumor

A

Cavernous hemangioma

61
Q

Cavernous hemangioma

A

Benign liver tumor. Consist of cavernous blood-filled vascular spaces lined by single epithelial layer. Do not biopsy due to risk for hemorrhage

62
Q

Most likely outcome of acute Hep C infection

A

Stable chronic hepatitis

Progression to cirrhosis is a close second

63
Q

What are brown pigment stones from?

A

Secondary to infection, which results in release of b-glucoronidase by injured hepatocytes and bacteria.

64
Q

How does prolonged parenteral nutrition cause gallstones?

A

Decreased CCK release because of lack of enteral stimulation

65
Q

Drug characteristics that allow for hepatic clearance into bile and stool

A

High lipophilicity, high volume of distribution

66
Q

Inhaled anethetic toxicity

A

Hepatotoxicity: either transferase elevation and no symptoms, or severe fulminant hepatitis. Hypersensitivity reaction. Liver atrophy, elevated transferases, prolonged ptt, leukocytosis, eosinophilia. Widespread necrosis and inflammation. Histo like filminant viral.

Note: albumin is not decreased because this is acute event.

67
Q

Hemochromatosis triad

A

skin hyperpigmentation, DM, pigment cirrhosis with hepatomegaly

“golden diabetes”

68
Q

Most common cause of hydatid cysts

A

Tapeworm echinococcus granulosus. Aspiration of cyst is not advised due to risk of anaphylactic shock

69
Q

Histo findings in acute viral hepatitis

A

Lymphocytic infiltrates, ballooning hepatocytes, hepatocyte necrosis, and apoptosis (with acidophilic apoptotic bodies)

70
Q

Microscopy findings in Reye syndrome

A

microvesicular steatosis, small fat vacuoles in cytoplasm

71
Q

Marker for evaluating cirrhotic pts for HCC

A

AFP

72
Q

Ballooning degeneration

A

Viral hepatitis

73
Q

Why do women present later with hemochromatosis?

A

Menstrual bleeding –> iron loss

74
Q

Why is there increased incidence in gall stones in pregnancy and OCPs?

A
  • Estrogen increases HMG-CoA reductase activity –> cholesterol hypersecretion
  • Progesterone induces gall bladder hypomotility
75
Q

Diffuse gallbladder calcification

A

Porcelain gallbladder, due to chronic cholecystitis, incidental finding. High rate of progression to gallbladder carcinoma

GI (6 decks)

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